Ginkgolic-Acid-Ginkgolic-acid-15-1-DataSheet-生命科學(xué)試劑-MedChemExpress

Hotline:400-820-3792Inhibitors?ScreeningLibraries?Proteinswww.MedChemEGinkgolicAcidCat.No.:HY-N0077CASNo.:22910-60-7Synonyms:Ginkgolicacid(15:1);GinkgolicacidI;Romanicardicacid分?式:C??H??O?分?量:346.5作?靶點(diǎn):E1/E2/E3Enzyme作?通路:MetabolicEnzyme/Protease儲(chǔ)存?式:Powder-20°C3years4°C2yearsInsolvent-80°C6months-20°C1month溶解性數(shù)據(jù)體外實(shí)驗(yàn)DMSO:100mg/mL(288.60mM;Needultrasonic)MassSolvent1mg5mg10mgConcentration制備儲(chǔ)備液1mM2.8860mL14.4300mL28.8600mL5mM0.5772mL2.8860mL5.7720mL10mM0.2886mL1.4430mL2.8860mL請(qǐng)根據(jù)產(chǎn)品在不同溶劑中的溶解度選擇合適的溶劑配制儲(chǔ)備液；?旦配成溶液，請(qǐng)分裝保存，避免反復(fù)凍融造成的產(chǎn)品失效。儲(chǔ)備液的保存?式和期限：-80°C,6months;-20°C,1month。-80°C儲(chǔ)存時(shí)，請(qǐng)?jiān)?個(gè)?內(nèi)使?，-20°C儲(chǔ)存時(shí)，請(qǐng)?jiān)?個(gè)?內(nèi)使?。體內(nèi)實(shí)驗(yàn)請(qǐng)根據(jù)您的實(shí)驗(yàn)動(dòng)物和給藥?式選擇適當(dāng)?shù)娜芙?案。以下溶解?案都請(qǐng)先按照InVitro?式配制澄的儲(chǔ)備液，再依次添加助溶劑：(為保證實(shí)驗(yàn)結(jié)果的可靠性，澄的儲(chǔ)備液可以根據(jù)儲(chǔ)存條件，適當(dāng)保存；體內(nèi)實(shí)驗(yàn)的?作液，建議您現(xiàn)?現(xiàn)配，當(dāng)天使?；以下溶劑前顯?的百分?指該溶劑在您配制終溶液中的體積占?；如在配制過(guò)程中出現(xiàn)沉淀、析出現(xiàn)象，可以通過(guò)加熱和/或超聲的?式助溶)1.請(qǐng)依序添加每種溶劑：10%DMSO>>40%PEG300>>5%Tween-80>>45%saline1/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemESolubility:≥2.75mg/mL(7.94mM);Clearsolution2.請(qǐng)依序添加每種溶劑：10%DMSO>>90%cornoilSolubility:≥2.75mg/mL(7.94mM);ClearsolutionBIOLOGICALACTIVITY?物活性GinkgolicAcid?種天然化合物，在體外實(shí)驗(yàn)中抑制SUMOylation的IC50為3.0μM。IC50&TargetIC50:3.0μM(SUMOylation)[1]體外研究GinkgolicacidinhibitstheinvitroSUMOylationofRanGAP1-C2withtheIC50valuesof3.0μM.ThelevelofSUMOylatedp53ismarkedlyreducedbytheginkgolicacidtreatment.Importantly,ginkgolicaciddoesnotaffectproteinubiquitinationincells.GinkgolicacidinhibitsthebindingbetweenE1andGA-BODIPYinadose-dependentmanner[1].Ginkgolicacid(31.2μg/mL)inhibitsHIVproteaseactivityby60%,comparedwiththenegativecontrol,andtheeffectisconcentration-dependent.Ginkgolicacidtreatment(50and100μg/mL)effectivelyinhibitsHIVinfectioninhumanPBMCcells.Ginkgolicacidattheconcentrationsupto150μg/mLdoesnotcauseanysignificantcytotoxicityinJurkatcells[2].GAonlyinhibitsthegrowthoftumorogeniccelllinesinabothdose-andtime-dependentmanner.TumorcellsaretreatedwithGAfor72h,70.53±4.54%Hep-2and63.5±7.2%Tca8113cellsareretardedatGO/G1phase,andthepercentageofapoptosisis40.4±1.58and38.4±1.7%,respectively.GA-treatedactivatedcaspase-3downregulatestheexpressionofanti-apoptoticBcl-2proteinandupregulatestheexpressionofpro-apoptoticBaxprotein,eventuallyleadingtoadecreaseintheBcl-2/BaxratiointumorcellsinhumanPBMCcells.Ginkgolicacidattheconcentrationsupto150μg/mLdoesnotcauseanysignificantcytotoxicityinJurkatcells[3].PROTOCOLCellAssay[2]Jurkatcells(106cells/mL)areculturedintheRPMImediumwithorwithoutdifferentconcentrationsofginkgolicacidfor48hourstotestthecytotoxicityofginkgolicacid.Thecytotoxicityofginkgolicacidisdeterminedusingatetrazoliumcompound(MTS)andanelectroncouplingreagent(PMS).MTSischemicallyreducedbycellsintoformazan,whichissolubleinthetissueculturemedium.Themeasurementoftheabsorbanceoftheformazancanbecarriedoutusing96wellmicroplatesat492nm.Sincetheproductionofformazanisproportionaltothenumberoflivingcells,theintensityoftheproducedcolorisagoodindicationoftheviabilityofthecells.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.戶使?本產(chǎn)品發(fā)表的科研?獻(xiàn)?NatCommun.2022Sep3;13(1):5204.?MolTherOncolytics.2019Dec14;16:86-99.?MicrobiolSpectr.2022Jan12;e0099121.?ToxicolApplPharmacol.2018Apr15;345:1-9.?Placenta.2022.2/3MasterofBioactiveMolecules—您?邊的抑制劑?師www.MedChemESeemorecustomervalidationsonwww.MedChemEREFERENCES[1].FukudaI,etal.GinkgolicacidinhibitsproteinSUMOylationbyblockingformationoftheE1-SUMOintermediate.ChemBiol.2009Feb27;16(2):133-40.[2].LüJM,etal.GinkgolicacidinhibitsHIVproteaseactivityandHIVinfectioninvitro.MedSciMonit.2012Aug;18(8):BR293-298.[3].ZhouC,etal.AntitumoreffectsofginkgolicacidinhumancancercelloccurviacellcyclearrestanddecreasetheBcl-2/Baxratiotoinduceapoptosis.Chemotherapy.2010;56(5):393-402.[4].QiuF,etal.PharmacologicalinhibitionofSUMO-1withginkgolicacidalleviatescardiacfibrosisinducedbymyocardialinfarctioninmice.ToxicolApplPharmacol.2018Apr15